Numerous investigators have demonstrated a pro-inflammatory role for complement in ischemia and reperfusion mediated myocardial injury. Additionally, anti-complement agents (including C1 esterase inhibitors, soluble CR1, and anti-CS antibody) have shown promise as therapy in human disease, especially for treatment of the inflammatory processes induced by coronary artery bypass surgery. However, the pathway(s) and mechanisms underlying these processes have not been clearly elucidated. Preliminary results from our laboratory indicate that the lectin complement pathway may play a significant role in complement mediated injury following oxidative stress. This proposal addresses the hypothesis that the lectin complement pathway is activated by myocardial ischemia and reperfusion which leads to the upregulation of leukocyte adhesion molecules. The specific aims of this proposal are to: 1) Characterize the contribution of the lectin complement pathway to complement activation following myocardial ischemia-reperfusion. 2) Characterize the effect of lectin complement pathway activation on the expression of adhesion molecules and neutrophil accumulation within the ischemic-reperfused myocardium. 3) Isolate, identify and characterize the ligand(s) that bind rat MBL within the heart.